biology essay

Noise Induced Hearing Loss Biology Essay

Published: 23, March 2015

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NIHL is a type of hearing loss developing from exposure to hazardous noise for months or years. The damage is caused by exposure to either consistent or impulse noise at levels of above 80 dB that leads to reduced ability to hear sounds. A typical notch at 4-6 KHz is seen in audiogram of NIHL patients.

Worldwide, 16% of the disabling hearing loss in adults is attributed to occupational noise, ranging from 7% to 21% in the various subregions by World Health Organization (WHO) [12].

Noise level and exposure time are key determinants for how noise affects hearing and how it can injure the ear;

High level, short duration noise exposure can stretch inner ear tissues and structures beyond their elastic limits, thus tearing them apart, or lower level, long duration noise exposure can fatigue the ear's delicate tissue. Overstimulation by intense sound gives rise to several structural and functional alterations in the organ of Corti. These changes include shrinking of the tectorial membrane [21], disruption of the tip-links of the stereocilia [22], fracture of the actin core and bending of the stereocilia[23, 24] , shortening and swelling of OHC bodies [25], contortion, blebbing, and degeneration of the cell body [26,27,], distension of the Deiters' cells (DCs) [28], swelling of afferent nerve endings [29, 30, 31] and Degeneration of afferent neurons [32].

2. NIHL and oxidative stress:

Noise induces production of reactive oxygen species (ROS) in the cochlea is now quite well characterized (Henderson), miller 2006). Different antioxidants enzymes are active in cochlea. Reactive Oxygen Species (ROS) & Reactive Nitrogen Species (RNS) are generated due to metabolic exhaustion in the cochlea leading to oxidative stress which damages tissues and organs. Antioxidant neutralise these ROS. The enzymes include Glutathione-s-transferase (GST), Catalase (CAT), Paraoxonases (PONx), Glutathione peroxidise (GPX), Glutathione reductase (GSR) and Superoxide dismutase (SOD). Ohlemiller et al. (1999b) (Bohne et al., 1999; Yamashita et al., 2004). Taken together, there is compelling evidence for a role of free radicals in NIHL and noise-induced sensory cell death. The ability of a variety of antioxidant agents to attenuate noise-induced hearing deficits and sensory cell loss is clear. Preclinical translational studies have confirmed the safety of multiple antioxidant agents, and many have been used in humans for years with few adverse effects reported.

YEAR

TITLE

MODEL USED

MATERIALS & METHOD

RESULT

CONCLUSION

Tatsuya Yamasoba et al

1998

Role of Glutathione in protection against NIHL.

Guinea Pigs

*Animals exposed at 102dB,3h, 5days and administration of BSO [inhibitor of GSH] and OTC [restores GSH] in two different groups.

*Animals were exposed to 4KHz, 105dB, 6h noise and given salicylate and NAC in combination.

*Significant reduction in hair cell loss seen.

*Reduction of NIHL using antioxidant compounds

2002

Protective effects of Phenyl-N-tert-butylnitrone on potentiation of NIHL by CO.

(Deepa Rao et al)

Rats

*Rats exposed to 100dB, 13.6KHz, 2h and administered PBN.

*Partial protection was observed in the protocols where PBN was injected following noise plus CO exposure.

* PBN administration appeared to reduce auditory impairment.

4. NIHL & related proteins:

The inner ear consists of cochlea which contains Organ of Corti where inner & outer hair cells along with hair like projections called stereocilia are present.

Tectorial membrane

The tectorial membrane is an extracellular matrix of the inner ear that is in contact with stereocilia bundles of specialized sensory hair cells. Sound induces movement of these hair cells relative to the tectorial membrane, deflects the stereocilia, and leads to fluctuations in hair-cell membrane potential, transducing electrical signals. Alpha-tectorine, beta- tectorine and otogelin, are glycoprotein, unique molecules from the inner ear have been associated with a moderate to severe deafness, which contacts the steriocilia bundles of specialized sensory hair cells with extracellular matrix of the tectorial membrane associated with pathophysiology of NIHL [46][47].

Mutation in TECT A gene is not fully understood & which produce an abnormally small protein by premature stop signal by instructions to alpha tectorine protein. Small concentration of Alpha Tectorine protein disturbs integrity of tectorine membrane required for conversion of sound to nerve impulses.

- tectorine and otogelin, are glycoprotein

Outer Hair Cell

Different proteins

Prestin is a motor membrane protein (an inbuilt amplifier), specifically expressed in outer hair cells of the cochlea and is essential for the auditory function [48]. Intracellular anions are thought to act as extrinsic voltage sensors, which bind to this protein and trigger the conformational changes required for rapid length changes in outer ear hair cells. Loss of this protein disturbs the balance in cochlea, characterized by moderate-to-severe hearing loss and deterioration of frequency selectivity which is voltage dependent applied across the OHC.

Setreocilia

I]Cadherin

The Cadherin 23 protein is involved in organization of hair bundles of stereocilia in IHC's & OHC's, promoting strong adhesion between them, and in Reissner's membrane. A change in this protein is characterized by moderate to profound high-frequency progressive sensorineural hearing loss [49]. in Chinese workers genetic polymorphism IN CDH23 gene plays an important role in the development of NIHL. Cadherin 23 is the candidate gene for suspetiblity of NIHL and polymorphism in this gene can be considered as risk factor for NIHL.

ii] Whirlin

Whirlin a protein involved in the elongation and maintenance (polymerization of actin for the growth of the membrane) of stereocilia in both IHCs and OHCs. Whirlin is expressed at stereocilia tips, known to play a key role in stereocilia development and loss of these proteins is responsible for profound deafness [51] [52].

Iii] Myosin

In the cochlea, Myosin localizes along the stereocilia, the inner and outer hair cells, and supporting cells, as well as in the synaptic terminals. Myosin is responsible for intracellular moments, structural defects of this protein causes consequent alterations in the auditory function. Myosin moves relative to actin filaments during the dynamic movements of stereocilia [53].

IV]Connexins

On the apical surface of outer hair cells, there are specialized stereocilia which deflects in response to sound. The deflection of stereocilia opens the transduction channels for ions through gap junctions. Connexins are a family of transmembrane proteins that form gap junctions between adjacent cells and allow intercellular communication. The association between connexin proteins and the inner ear is well established [54].

The abundant expression of connexins in the auditory system of the inner ear demonstrates their importance in inner ear development and the hearing process. Most compelling, there are remarkable changes in the connexins that are associated with deafness. Important is the involvement of connexion 26 in hearing loss. It controls ions movement from channels, allowing inflow of potassium from the endolymph to inner and outer hair cells of the cochlea causing depolarization of cell membrane. The subsequent influx of calcium causes release of neurotransmitters from the synaptic vesicles on to the primary afferent nerve ending synapses.

VI} Head Shock Proteins

Heat shock proteins are a class of functionally related proteins that are introduced by physical and physiological stresses, including heat and noise. In a three polymorphisms (rs1043618, rs1061581 and rs2227956) in hsp70 genes were genotyped in 206 Swedish and 238 Polish DNA samples of noise-exposed workers. The study found rs2227956 in hsp70 to be significantly associated with hearing loss in both sample sets. Also rs1043618 and rs1061581 were significant in the Swedish sample set but not in the Polish sample set [55].The studies on the other proteins in NIHL have been summarized below:

YEAR

TITLE

MODEL USED

MATERIALS & METHOD

RESULT

CONCLUSION

2008

Bcl-2 genes regulate NIHL.

(Daisyke Yamashita et al)

Guinea Pigs

*Animals exposed to 4Khz,120dB, ABR assessed.

*Assessment of expressions of anti- and proap optic Bcl-2 genes was done.

*Loss of OHC's seen in PTS.

*Bcl-Xl expressed in TTS exposure.

*Bak expressed in PTS exposure.

*Bcl-xL plays an essential role in prevention of sensory cell death following TTs levels.

*PTS exposure proves expression of Bak.

2003

The caspase pathway in noise induced apoptosis of the chinchilla cochlea.

(Thomas Nicotera et al)

Chinchilla

*Chinchillas were exposed to 110 dB for 1hr.

*Detection of active caspases

*Tunnel assay for DNA fragmentation.

*Microscopy of organ of corti

* OHC's & IHC's exhibited apoptotic and necrotic changes.

* Activation of caspase 3,8, 9 detected in OHC's.

* Translocation of cyt C from mitochondria.

*Cyt C is associated with both apoptotic and necrotic pathway

* Caspases are associated with apoptotic cell death programme.

2004

Calcineurin activation contributes to NIHL.

(Shujiro Minami et al )

Guinea pigs

*Animals exposed to noise (4 KHz,120dB,5h)

*Immunocytochemistry for calceneurin and Rhodamine phalloidin.

*Propidium iodide (PI) staining of hair cells.

*Local application of the calceneurin inhibitors,FK506 and Cyclosporin A

*Calceneurin immunoreactivity present in OHC's.

*FK506 and cyclosporine A reduce hair cell loss

*Calcineurin is associated with dying hair cells.

*Calcineurin inhibitors are of potential therapeutic value for protection and function of Organ of Corti against noise trauma.

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